scholarly journals Faculty Opinions recommendation of Increased human intestinal barrier permeability plasma biomarkers zonulin and FABP2 correlated with plasma LPS and altered gut microbiome in anxiety or depression.

2020 ◽  
Author(s):  
Alessio Fasano
Keyword(s):  
Gut Microbiome ◽  
Intestinal Barrier ◽  
Barrier Permeability ◽  
Plasma Biomarkers

scholarly journals Increased human intestinal barrier permeability plasma biomarkers zonulin and FABP2 correlated with plasma LPS and altered gut microbiome in anxiety or depression

Gut ◽  
2017 ◽  
Vol 67 (8) ◽  
pp. 1555.2-1557 ◽  
Author(s):  
Bruce R Stevens ◽  
Ruby Goel ◽  
Kim Seungbum ◽  
Elaine M Richards ◽  
Richard C Holbert ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
Intestinal Barrier ◽  
Barrier Permeability ◽  
Plasma Biomarkers

The gut and cardiovascular diseases

ESC CardioMed ◽  
2018 ◽  
pp. 1090-1093
Author(s):  
Giuseppe Rosano
Keyword(s):  
Heart Failure ◽  
Cardiovascular Diseases ◽  
Gut Microbiome ◽  
Intestinal Barrier ◽  
Therapeutic Approaches ◽  
Barrier Permeability ◽  
New Therapeutic Approaches ◽  
Obesity And Diabetes ◽  
Gut Homeostasis ◽  
Progression Of Atherosclerosis

The physiological functioning of the gut is central for the pharmacokinetics of orally administered cardiovascular drugs and alteration of the gut homeostasis may have relevant repercussions on the effect of these drugs. The gut microbiome may affect the absorption and metabolism of nutrients favouring the development of obesity and diabetes. Furthermore, alterations in intestinal barrier permeability lead to the penetration of bacteria and bacterial wall products into the circulation and may contribute to the progression of atherosclerosis and worsening of heart failure. Despite the suggestions of the possible interaction between the gut and the cardiovascular system and of stimulating novel mechanisms for disease progression that may open to new therapeutic approaches, the available evidence must be considered preliminary.

scholarly journals Gut Microbiome in Psoriasis: An Updated Review

Pathogens ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 463
Author(s):  
Mariusz Sikora ◽  
Albert Stec ◽  
Magdalena Chrabaszcz ◽  
Aleksandra Knot ◽  
Anna Waskiel-Burnat ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
Beta Diversity ◽  
Large Scale ◽  
Skin Diseases ◽  
Intestinal Barrier ◽  
Alpha Diversity ◽  
Current Data ◽  
Intestinal Microbiome ◽  
Microbial Composition ◽  
Alpha And Beta Diversity

(1) Background: A growing body of evidence highlights that intestinal dysbiosis is associated with the development of psoriasis. The gut–skin axis is the novel concept of the interaction between skin diseases and microbiome through inflammatory mediators, metabolites and the intestinal barrier. The objective of this study was to synthesize current data on the gut microbial composition in psoriasis. (2) Methods: We conducted a systematic review of studies investigating intestinal microbiome in psoriasis, using the PRISMA checklist. We searched MEDLINE, EMBASE, and Web of Science databases for relevant published articles (2000–2020). (3) Results: All of the 10 retrieved studies reported alterations in the gut microbiome in patients with psoriasis. Eight studies assessed alpha- and beta-diversity. Four of them reported a lack of change in alpha-diversity, but all confirmed significant changes in beta-diversity. At the phylum-level, at least two or more studies reported a lower relative abundance of Bacteroidetes, and higher Firmicutes in psoriasis patients versus healthy controls. (4) Conclusions: There is a significant association between alterations in gut microbial composition and psoriasis; however, there is high heterogeneity between studies. More unified methodological standards in large-scale studies are needed to understand microbiota’s contribution to psoriasis pathogenesis and its modulation as a potential therapeutic strategy.

scholarly journals Renal Denervation Attenuates Neuroinflammation in the Brain by Regulating Gut-Brain Axis in Rats With Myocardial Infarction

2021 ◽  
Vol 8 ◽  
Author(s):  
Jun-Yu Huo ◽  
Wan-Ying Jiang ◽  
Yi-Ting Lyu ◽  
Lin Zhu ◽  
Hui-Hui Liu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Inflammatory Cytokines ◽  
Renal Denervation ◽  
Intestinal Barrier ◽  
Intestinal Injury ◽  
Microglia Activation ◽  
Barrier Permeability ◽  
Microbial Dysbiosis ◽  
Cardiac Functions ◽  
The Brain

Aims: The development of neuroinflammation deteriorates the prognosis of myocardial infarction (MI). We aimed to investigate the effect of renal denervation (RDN) on post-MI neuroinflammation in rats and the related mechanisms.Methods and Results: Male adult Sprague-Dawley rats were subjected to sham or ligation of the left anterior descending coronary artery to induce MI. One week later, the MI rats received a sham or RDN procedure. Their cardiac functions were analyzed by echocardiography, and their intestinal structures, permeability, and inflammatory cytokines were tested. The intestinal microbiota were characterized by 16S rDNA sequencing. The degrees of neuroinflammation in the brains of rats were analyzed for microglia activation, inflammatory cytokines, and inflammation-related signal pathways. In comparison with the Control rats, the MI rats exhibited impaired cardiac functions, intestinal injury, increased intestinal barrier permeability, and microbial dysbiosis, accompanied by increased microglia activation and pro-inflammatory cytokine levels in the brain. A RDN procedure dramatically decreased the levels of renal and intestinal sympathetic nerve activity, improved cardiac functions, and mitigated the MI-related intestinal injury and neuroinflammation in the brain of MI rats. Interestingly, the RDN procedure mitigated the MI-increased intestinal barrier permeability and pro-inflammatory cytokines and plasma LPS as well as ameliorated the gut microbial dysbiosis in MI rats. The protective effect of RDN was not significantly affected by treatment with intestinal alkaline phosphatase but significantly reduced by L-phenylalanine treatment in MI rats.Conclusions: RDN attenuated the neuroinflammation in the brain of MI rats, associated with mitigating the MI-related intestinal injury.

scholarly journals Gut Microbiome, Intestinal Permeability, and Tissue Bacteria in Metabolic Disease: Perpetrators or Bystanders?

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1082 ◽  
Author(s):  
Rima M. Chakaroun ◽  
Lucas Massier ◽  
Peter Kovacs
Keyword(s):  
Metabolic Disease ◽  
Intestinal Permeability ◽  
Systemic Inflammation ◽  
Gut Microbiome ◽  
Metabolic Diseases ◽  
Treatment Strategies ◽  
Intestinal Barrier ◽  
Intestinal Bacteria ◽  
Current Evidence ◽  
Microbial Culture

The emerging evidence on the interconnectedness between the gut microbiome and host metabolism has led to a paradigm shift in the study of metabolic diseases such as obesity and type 2 diabetes with implications on both underlying pathophysiology and potential treatment. Mounting preclinical and clinical evidence of gut microbiota shifts, increased intestinal permeability in metabolic disease, and the critical positioning of the intestinal barrier at the interface between environment and internal milieu have led to the rekindling of the “leaky gut” concept. Although increased circulation of surrogate markers and directly measurable intestinal permeability have been linked to increased systemic inflammation in metabolic disease, mechanistic models behind this phenomenon are underdeveloped. Given repeated observations of microorganisms in several tissues with congruent phylogenetic findings, we review current evidence on these unanticipated niches, focusing specifically on the interaction between gut permeability and intestinal as well as extra-intestinal bacteria and their joint contributions to systemic inflammation and metabolism. We further address limitations of current studies and suggest strategies drawing on standard techniques for permeability measurement, recent advancements in microbial culture independent techniques and computational methodologies to robustly develop these concepts, which may be of considerable value for the development of prevention and treatment strategies.

scholarly journals Astrovirus Increases Epithelial Barrier Permeability Independently of Viral Replication

2007 ◽  
Vol 81 (21) ◽  
pp. 11937-11945 ◽  
Author(s):  
Lindsey A. Moser ◽  
Michael Carter ◽  
Stacey Schultz-Cherry
Keyword(s):  
Viral Replication ◽  
Protein A ◽  
Intestinal Barrier ◽  
Intestinal Damage ◽  
Barrier Permeability ◽  
Culture Model ◽  
Junction Protein ◽  
Serotype 1 ◽  
Human Astrovirus

ABSTRACT Astrovirus infection in a variety of species results in an age-dependent diarrhea; however, the means by which astroviruses cause diarrhea remain unknown. Studies of astrovirus-infected humans and turkeys have demonstrated few histological changes and little inflammation during infection, suggesting that intestinal damage or an overzealous immune response is not the primary mediator of astrovirus diarrhea. An alternative contributor to diarrhea is increased intestinal barrier permeability. Here, we demonstrate that astrovirus increases barrier permeability in a Caco-2 cell culture model system following apical infection. Increased permeability correlated with disruption of the tight-junction protein occludin and decreased the number of actin stress fibers in the absence of cell death. Additionally, permeability was increased when monolayers were treated with UV-inactivated virus or purified recombinant human astrovirus serotype 1 capsid in the form of virus-like particles. Together, these results demonstrate that astrovirus-induced permeability occurs independently of viral replication and is modulated by the capsid protein, a property apparently unique to astroviruses. Based on these data, we propose that the capsid contributes to diarrhea in vivo.

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